It is known that H. pylori infection triggers a pathological progression in gastric mucosa, which eventually culminates in the development of gastric cancer. Inevitably, the infection causes an inflammatory response in the host, which generates reactive oxygen species and nitrogen, which may cause protein alterations, damage to cell membranes and oxidation DNA molecule, which are known to be important steps in the development of gastric cancer. In addition, there is evidence in the literature and obtained by our research group, showing that infection with H. pylori is directly linked to a reduction in the efficiency of DNA repair mechanisms, which would favor the accumulation of mutations and genomic instability, favoring the genesis of gastric cancer. Some recent studies show the importance of regulating via oncogenic Wnt/b-catenin in various types of cancer. However, the association between b-catenin in the DNA repair pathways are still poorly explored, especially in gastric carcinogenesis. We intend to evaluate the possible regulatory role of b-catenin in MMR genes modulated by H. pylori.
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